title: High frequencies of CD158b+ NK cells are associated with persistent hepatitis C virus infections.
abstract: BACKGROUND
  During the early phases of a hepatitis C virus (HCV) infection, NK cell activation appears to be critical to the induction of adaptive immune responses that have the potential of clearing the infection. This study aimed to investigate the phenotype and function of NK cells in chronic HCV (CHC) patients, particularly patients who cleared HCV infections spontaneously (SR-HCV).
  
  
  METHODS
  Peripheral blood NK cells were compared between 36 CHC patients, 12 SR-HCV patients, and 14 healthy controls (HC). The phenotype and function of NK cells were characterized by flow cytometry. In addition, the potential associations between the frequency of NK cell subsets and ALT, AST and HCV viral loads were also analyzed.
  
  
  RESULTS
  Our data revealed that the population of CD3-CD56+ NK cells was significantly decreased in CHC and SR-HCV patients compared to levels in HC (P = 0.031, P = 0.014). Interestingly, we found that the levels of the CD158b inhibitory receptor were higher in CHC patients compared to levels observed in HCand SR-HCV subjects (P = 0.018, P = 0.036). In addition, the percentages of the activation receptors NKp30 and NKp46 were significantly decreased in CHC and SR-HCV patients compared to their expression levels in HC (P < 0.05). Moreover, the frequencies of inducible CD107a (but not IFN-γ-secreting) NK cellsfrom both CHC and SR-HCV patients were significantly lower than frequencies observed in controls (P = 0.018, P = 0.027).
  
  
  CONCLUSIONS
  Our data indicated that the higher frequency of inhibitory NK cells combined with fewer activated NK cells may be associated with HCV-related chronic inflammation involved in CHC pathogenesis.
authors.affiliation: Department of Central Laboratory, the Second Part of First Hospital, Jilin University, Changchun 130031, China.
authors.forename: Hui-Fan
authors.initials: HF
authors.lastname: Ji
authors.forename: Juan
authors.initials: J
authors.lastname: Wang
authors.forename: Lei
authors.initials: L
authors.lastname: Yu
authors.forename: Jun-Qi
authors.initials: JQ
authors.lastname: Niu
authors.forename: Desalegn Admassu
authors.initials: DA
authors.lastname: Ayana
authors.forename: Yan-Fang
authors.initials: YF
authors.lastname: Jiang
mesh_terms: D056704:Adaptive Immunity; D000328:Adult; D000368:Aged; D000410:Alanine Transaminase / Q000097:blood; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D005260:Female; D005434:Flow Cytometry; D019698:Hepatitis C, Chronic / Q000097:blood / Q000175:diagnosis / Q000276:immunology*; D006801:Humans; D016130:Immunophenotyping / Q000379:methods; D007694:Killer Cells, Natural / Q000276:immunology* / Q000821:virology; D008213:Lymphocyte Activation; D018655:Lymphocyte Count; D051907:Lysosomal Membrane Proteins / Q000097:blood; D008297:Male; D008875:Middle Aged; D055627:Natural Cytotoxicity Triggering Receptor 1 / Q000097:blood; D055628:Natural Cytotoxicity Triggering Receptor 3 / Q000097:blood; D010641:Phenotype; D054344:Receptors, KIR2DL3 / Q000097:blood*; D055815:Young Adult; D052118:Lysosomal-Associated Membrane Protein 1
chemical_list: D000410:Alanine Transaminase; D015415:Biomarkers; D051907:Lysosomal Membrane Proteins; D055627:Natural Cytotoxicity Triggering Receptor 1; D055628:Natural Cytotoxicity Triggering Receptor 3; D054344:Receptors, KIR2DL3; C515078:KIR2DL3 protein, human; C489116:LAMP1 protein, human; D052118:Lysosomal-Associated Membrane Protein 1; C112260:NCR1 protein, human; C431710:NCR3 protein, human